Mysterious TREM2 receptor destroys Alzheimer’s

Mysterious TREM2 receptor destroys Alzheimer’s

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“Remarkable” – that’s how researchers are describing this new study associated with ending Alzheimer’s and having a clear and quick mind as we age

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Mysterious TREM2 receptor destroys Alzheimer’s

A series of exciting experiments shows how the immune system interacts with Alzheimer’s disease.

Scientists have identified a receptor that destroys the tangled protein structures that are thought to cause Alzheimer’s.

They also found a way to upregulate the receptor and treat Alzheimer’s symptoms in animal models.

These two studies were conducted at the Sanford Burnham Prebys Medical Research Institute and published in the journal Neuron.

The first paper set out to investigate a receptor (TREM2) that is associated with changes in Alzheimer’s risk in humans.

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“Mutations in TREM2 are linked to increased Alzheimer’s risk.”

TREM2 is a cell receptor – it is active in the brain.

This study set out to figure out the function of TREM2.

“Neurobiological functions of TREM2 and its pathophysiological ligands remain elusive.”

The TREM2 receptor binds to the structures that are thought to cause Alzheimer’s disease.

These structures are made up of deformed and tangled proteins.

They trap amyloid plaques.

“Here we found that TREM2 directly binds to amyloid plaques.”

TREM2 was not only trapping amyloid plaques – it was destroying them.

The research team identified the process through which the body can destroy Alzheimer’s and cause amyloid-beta plaques.

“Our first paper identifies how amyloid-beta binds to TREM2 and activates immune cells to degrade amyloid-beta.”

The second paper built on these impressive results…

In this series of experiments, the researchers wanted to find out if increasing the TREM2 receptor could fight Alzheimer’s disease.

The researchers bred mutant mice to have higher levels of the TREM2 receptor.

“To study whether increasing TREM2 could modify the disease we developed transgenic mice expressing human TREM2.”

The study found that they could reduce Alzheimer’s-related amyloid plaques by increasing TREM2 via genetic modification.

“We found that elevated TREM2 expression reduced amyloid burden in the mutant mouse model.”

But what really matters is the change in cognitive performance!

Increasing TREM2 also fought Alzheimer’s symptoms in the mouse model.

“Elevated TREM2 led to improved memory performance in Alzheimer’s disease models.”

The study proves that changing the levels of TREM2 has a direct effect on Alzheimer’s – it destroys the amyloid plaques and it improves symptoms of Alzheimer’s.

“An increase in TREM2 expression ameliorates neuropathological and behavioral deficits in Alzheimer’s disease mouse models.”

Scientists already knew that people with low levels of TREM2 were more likely to develop Alzheimer’s disease.

We now know that this is because TREM2 is a detoxification system for Alzheimer’s plaques.

This study also adds more weight to the idea that amyloids caused by the plaques are a cause of Alzheimer’s disease.

Though this has been mainstream thought for quite some time, it has not been entirely proven.

We still have to figure out a safe way to upregulate TREM2 in humans with Alzheimer’s disease.

Increasing TREM2 does have some risks.

If TREM2 is over-activated, it will signal for inflammatory cytokines – proteins that could cause inflammatory damage to the brain and other tissues.

It’s early days, but these are exciting discoveries.

You should see a healthcare professional about diagnosing and treating Alzheimer’s disease.

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Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.
TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function http://www.cell.com/neuron/fulltext/S0896-6273(18)30056-4?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627318300564%3Fshowall%3DtrueThe brain's immune system may be key to new Alzheimer's treatments https://medicalxpress.com/news/2018-03-brain-immune-key-alzheimer-treatments.htmlElevated TREM2 Gene Dosage Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer’s Disease Models http://www.cell.com/neuron/fulltext/S0896-6273(18)30101-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627318301016%3Fshowall%3Dtrue

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